中枢性低钠血症的诊治体会

目的：分析探讨中枢性低钠血症的诊断及处理方法。方法：回顾性分析我科近5年收治的32例中枢性低钠血症患者诊治经过。结果：本组5例符合抗利尿激素分泌异常综合征（SIADH）,27例符合脑性耗盐综合征（CSWS）,全部患者低钠血症在1-2周内均得到纠正。结论：神经外科疾患并发中枢性低钠血症应密切监测血钠、中心静脉压及24h尿钠水平,并以此为依据鉴别其类型,给予有效治疗。     

鞍区肿瘤术后低钠血症的临床处理

目的 探讨鞍区肿瘤术后抗利尿激素分泌异常综合征（SIADH）及脑性盐耗综合征（CSWS）的鉴别诊断及治疗方法。方法 回顾性分析86例首次接受鞍区肿瘤术后低钠血症患者的临床表现和实验室检查,总结有效的诊断及治疗方法。将48例垂体腺瘤患者分为A组,28例颅咽管瘤和10例脑膜瘤患者分为B组;CSWS低钠者补钠、迅速扩容、补充高渗盐水,SIADH低钠者限水补盐利尿治疗。结果 诊断为SIADH的39例,CSWS的47例。1例于术后8 d死亡;1例出院后1个月发生低钠血症死亡;2例患者因水中毒出现抽搐、昏迷,对症治疗1个月后出院;余82例治疗后恢复良好。结论 当鞍区肿瘤术后的患者合并低钠血症时应先排除医源性因素,细胞外容量是区别SIADH与CSWS的可靠指标,体质量及中心静脉压检测简单有效。     

Fluid and electrolyte management: putting a plan in motion

Fluid and electrolyte management is challenging for clinicians, as electrolytes shift in a variety of settings and disease states and are dependent on osmotic changes and fluid balance. The development of a plan for managing fluid and electrolyte abnormalities should start with correcting the underlying condition. In most cases, this is followed by an assessment of fluid balance with the goal of achieving euvolemia. After fluid status is understood and/or corrected, electrolyte imbalances are simplified. Many equations are available to aid clinicians in providing safe recommendations or at least to give a starting point for correcting the abnormalities. However, these equations do not take into consideration the vast differences between clinical scenarios, thus making electrolyte management more challenging. The supplementation plan, whether delivered intravenously or orally, must include an assessment of renal and gastrointestinal function, as most guidelines are established under the assumption of normal digestion, absorption and excretion. After the plan is developed, frequent monitoring is vital to regain homeostasis. A fluid and electrolyte management plan developed by a multidisciplinary team is advantageous in promoting continuity of care and producing safe outcomes.     

慢性重型肝炎并发肝肾综合征的相关因素分析

目的分析慢性重型肝炎并发肝肾综合征（HRS）的发病率,研究慢性重型肝炎伴HRS患者与单纯性慢性重症肝炎患者的临床资料和血液生化指标,探讨慢性重型肝炎并发HRS的因素。方法回顾性分析我院2008年1月至2010年10月因慢性重型肝炎住院患者共450例。根据患者住院期间是否发生HRS。将研究对象分成慢性重型肝炎伴HRS（HRS组,105例）和单纯慢性重型肝炎组（非HRS组,345例）。比较两组患者的Child—Pugh分级、终末期肝病评分（MELD）、腹水发生率和血液生化指标。结果慢性重型肝炎并发HRS的院内发病率为23．3％。HRS组MELD评分为31．7±4．5,高于对照组的26．3±6．8（t=-2．45。P〈0．05）,腹水发生率为100％,高于对照组的33．9％（X。=140．65,P〈0．01）。HRS组Alb为（27．3±3．2）g／L,低于非HRs组（34．8±3．6）g／L（t=-10．03,P〈0．01）。HRS组血钠水平为（128．5±7．5）mmol／L,明显低于对照组的（137．4±6．5）mmol／L（t=-4．72。P〈0．01）。HRS组的TBi1、DBi1、AST、ALT、BUN、Cr高于非HRS组（州直分别为3．75、3．65、2．58、2．51、11．47、7．86．P〈0．05）。而TP、Na、cl低于非HRS组（州直分别为3．83、4．72、2．74,P〈0．05）,ALP、GGT、K在两组间差异无统计学意义（P〉0．05）。结论低白蛋白血症和低钠血症是慢性重型肝炎并发HRS的重要因素。     

颅脑损伤并发中枢性低钠血症的诊治体会

目的:分析总结颅脑损伤并发中枢性低钠血症的临床特点与病因,对其发病机制与诊断治疗进行探讨.方法:对我院2000年1月～2009年12月收治的86例颅脑损伤并发中枢性低钠血症患者的临床资料进行回顾性分析.结果:86例患者中出现脑性盐耗综合症(CSWS)的患者有62例,出现抗利尿激素异常分泌综合征(SIADH)患者24例....     

Increased aquaporin-1 and Na+ -K+ -2Cl- cotransporter 1 expression in choroid plexus leads to blood-cerebrospinal fluid barrier disruption and necrosis of hippocampal CA1 cells in acute rat models of hyponatremia

Hyponatremia is a metabolic disorder characterized by increased cerebrospinal fluid (CSF) volume and pressure, although the site of brain insult is unclear. Specifically, the hippocampus, which is in direct contact with expanding CSF ventricles, may be involved. The present study was undertaken to investigate the possible roles of choroid plexus aquaporin-1 (AQP1) and of cation chloride transporters (Na(+) -K(+) -2Cl(-) cotransporter 1 [NKCC1] and K(+) -Cl(-) cotransporter 4 [KCC4]) in the underlying hippocampal pathophysiology of hyponatremia in acute (6 and 12 hr duration) experimental models. It was found that the expressions of AQP1 and NKCC1 proteins in choroid plexus were significantly increased, whereas the expression of KCC4 protein was unchanged vs. control values after 6 and 12 hr of hyponatremia. Choroid plexuses with increased AQP1 and NKCC1 after 6 hr of hyponatremia showed caspase 3-dependent apoptosis and disruption of the blood-CSF barrier. Furthermore, necrotic changes in CA1 neuronal cells were observed after 6 and 12 hr of hyponatremia. Overall, these data suggest that increases in AQP1 and NKCC1 expression under hyposmotic stress may be one of the molecular mechanisms underlying the pathophysiology of acute hyponatremia, such as the necrotic cell death of hippocampal CA1 region by increasing water transport across the blood-CSF barrier. Furthermore, we suggest that opening of the blood-CSF barrier after acute hyponatremia may be triggered the secondary adverse conditions that are capable of enhancing selective necrosis in hippocampal CA1 cells.     

急性心肌梗死伴低钠血症的临床意义

目的探讨急性心肌梗死(AM I)患者并发低钠血症的临床意义。方法对我院2008年1月—2009年7月129例AM I患者进行了回顾性分析,根据患者入院后即刻血清钠离子浓度水平分为两组:低钠血症组(Na+(135 mmol/L)和血钠正常组(Na+≥135 mmol/L)。比较两组病人血清钠离子浓度与年龄、病史、梗死面积及并发症的关系。结果低钠血症的发生率为31.8%(41/129),<60岁的占58.5%(24/41)。无心绞痛病史者占63.4%(26/41),与血钠正常组比较差异有统计学意义,心肌梗死面积两组间差异无统计学意义。而且,有53.7%(22/41)病人在血清心肌酶尚未升高时即出现了低钠血症。结论低钠血症是AM I的常见合并症,主要由于机体的应激反应所致,过度的应激反应可能是AM I预后不良的原因之一,因此低钠血症的病人更应尽早抗应激治疗。     

Life-threatening heat-related illness with severe hyponatremia in an aluminum smelter worker

Heat stress is a recognized occupational hazard in aluminum smelter pot rooms. This is the report of an unusual and complex case of heat-related illness in an aluminum smelter worker. The 34-year-old male US worker developed life-threatening heat-related illness in August 2018, on his first day back at work after a 7-day absence. The worker initially presented with bilateral hand then all-extremity cramping followed some hours later by a generalized seizure and acute mental status changes, including combativeness. Emergency room evaluation identified a serum sodium level of 114 mmol/L. Acute liver and kidney injury ensued along with profound rhabdomyolysis, with peak total creatinine phosphokinase level reaching over 125 000 units/L at 3 days post incident. Initial ventilatory support, careful fluid resuscitation, and electrolyte management were provided. Metabolic encephalopathy resolved. Complications included sepsis. After 5 days in the intensive care unit and eight additional days of inpatient management, observation, and the initiation of rehabilitation, the worker was discharged. Residual effects include polyneuropathy of upper and lower extremities and the postdischarge magnetic resonance imaging finding of a cerebellar lesion. Prevailing considerations in the differential diagnosis included exertional heat stroke and/or exertion-associated hyponatremia with encephalopathy.